1. Twenty-five patients with mild essential hypertension, identified during a survey of a population born in 1936, were investigated.

2. Basal and post-frusemide values for plasma renin concentration and plasma angiotensin II concentration did not differ markedly from reference values in 25 40-year-old control subjects. In the untreated, sodium replete state saralasin infusion (5·4 nmol min−1 kg−1) produced an increase in mean arterial pressure in the patient group as a whole.

3. Twenty-one patients were treated with hydrochlorothiazide, mean dose 75 mg/day for 3 months. Pre-treatment, frusemide-stimulated plasma renin concentration and plasma angiotensin II, and values during thiazide treatment were higher in ‘non-responders’ (n = 10) to hydrochlorothiazide treatment than in ‘thiazide-responders’ (n = 11). During thiazide therapy, angiotensin II blockade induced a clear-cut decrease in mean arterial pressure in all ‘thiazide-nonresponders’ whereas only four out of 11 ‘thiazide-responders’ showed a borderline decline in mean arterial pressure.

4. The functional significance of the renin—angiotensin system in mild essential hypertension emerges only after thiazide treatment. Thiazide-induced stimulation of the renin—angiotensin system counter-balanced the hypotensive effect of thiazide in some 40% of the treated patients. Thus the responsiveness of the renin—angiotensin system determined the blood pressure response to thiazide treatment.

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